Depolarizing neuromuscular blocking

E. Succinylcholine is the only depolarizing neuromuscular blocking in widespread clinical use, particularly as an aid for intubation. Its administration may produce muscle fasciculation and postoperative muscle pain. It can produce hyperkalemia in patients with muscle damage or prolonged paralysis in patients with atypical plasma cholinesterase. 

Mechanism of Action A depolarizing neuromuscular blocking agent that causes the release of acetylcholine and inhibits cholinesterase. Therapeutic Effect Results in a spastic paralysis of the worm and consequent expulsion from the host s intestinal tract. 

Both pyrantel (13a) and morantel (13b) are depolarizing neuromuscular blocking agents that stimulate ganglia and also possess acetylcholine-like actions on smooth muscle. 

Mechanism of action of depolarizing neuromuscular blocking drugs. 

Pyrantel pamoate [pi RAN tel] along with mebendazole is effective in the treatment of infections caused by roundworms, pinworms (see Figure 36.4), and hookworms. Pyrantel pamoate is poorly absorbed orally and exerts its effects in the intestinal tract. It acts as a depolarizing neuromuscular blocking agent, causing persistent... 

A variety of other tropane alkaloids have been isolated of which the most important is anatoxin-A, a highly toxic nACh-R agonist and depolarizing neuromuscular blocking agent deriving from Anabaena cyanobacterium species that can contaminate inland waters. 

Driessen JJ, Vree TB, van Egmond J, Booij LH, Crul JF. Interaction of midazolam with two non-depolarizing neuromuscular blocking drugs in the rat in vivo sciatic nerve-tibialis anterior muscle preparation. Br J Anaesth 1985 57(ll) 1089-94. 

Hughes R, Chappie DJ. Effects on non-depolarizing neuromuscular blocking agents on peripheral autonomic mechanisms in cats. Br J Anaesth 1976 48(2) 59-68. 

Burns are associated with resistance to atracurium (43), as for several other non-depolarizing neuromuscular blocking agents. The EC50 is increased and dose requirements may be increased by up to 2-3 times. The resistance varies with the burn area and the time from injury (SEDA-12, 116), being maximal at 15 0 days in patients repeatedly anesthetized. 

In contrast to reports on other non-depolarizing neuromuscular blocking agents, resistance to atracurium has not been found in patients taking long-term carbamazepine (SEDA-13, 104) (58). 

From animal experiments (8) it seems hkely that drug interactions with atracurium will be similar to those for other non-depolarizing neuromuscular blocking agents. Laudanosine has been reported to increase the MAC for halothane in animals (61). 

Hughes R, Payne JP, Sngai N. Stndies on fazadinium bromide (AH 8165) a new non-depolarizing neuromuscular blocking agent. Can Anaesth Soc J 1976 23(l) 36-47. 

The effects of non-depolarizing neuromuscular blocking drugs can be potentiated and their actions prolonged by large doses of local anesthetics, because of depression of nerve conduction, inhibition of acetylcholine formation, mobilization, and release, reduced postsynaptic receptor channel opening times, and reduced muscle contraction (370). 

Wierda JM, Kleef UW, Lambalk LM, Kloppenburg WD, Agoston S. The pharmacodynamics and pharmacokinetics of Org 9426, a new non-depolarizing neuromuscular blocking agent, in patients anaesthetized with nitrous oxide, halothane and fentanyl. Can J Anaesth 1991 38(4 Pt l) 430-5. 

Patients with burns require more D-tubocurarine (and higher plasma concentrations) for the same degree of blockade compared with non-burned patients (6). The mechanism is not known, but it appears not to be altered pharmacokinetics (7). The resistance to non-depolarizing neuromuscular blocking agents (SEDA-8,136) appears to be influenced by the size of the body surface area burned and by the time which has elapsed since the injury (see Atracurium). In extensive burns dose requirements are increased approximately by a factor of 2-3. 

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